sinco mark

8/14/2019 sinco mark

1/22


2/22

GUILLAIN BARRE

SYNDROMEA CASE PRESENTATION


3/22


4/22

disorder wherein the bodys own immune system attacksthe peripheral nerves that convey sensory information(e.g., pain, temperature) from the body to the brain andmotor (i.e., movement) signals from the brain to thebody. It is a rare condition occurring once in every

100,000 people per year but it is one of the leadingcauses of non-trauma induced paralysis in the world.Exactly what triggers Guillain-Barre syndrome isunknown and it may occur at any age but is mostcommon among young adults and the elderly. The

condition is often preceded by either a viral or bacterialinfection of the lungs or gastrointestinal tract. Signs ofthe original infection have already disappeared before thesymptoms of Guillain-Barre begin.

People with GBS usually have muscle weakness orparalysis that starts in the legs and feet. It progresses uptoward the arms and head. Sometimes the weaknessstarts in the arms and moves downward. Occasionally, it

starts in the arms and legs at the same time. The spreadfrom feet to head can occur within 24 to 72 hours but cantake longer. Mild cases of Guillain-Barre syndrome maypresent only with ataxia (difficulty in walking andbalancing), whereas severe cases may present withdifficulty in respiration due to paralysis of the respiratorymuscles and cranial nerves.


5/22

rea men or u a n- arre yn rome cons s s osupportive care, ventilatory management (in about onethird of patients), and specific therapy with intravenousimmunoglobulin or plasmapheresis. However, each caseof Guillain-Barre' Syndrome is different. It is important to

realize that the complications and therefore treatments ofGuillain-Barre' syndrome are not predictable. For themost part, treatments are highly individualized.Our patient is Mr. C, a seventeen year old first year highschool student of Loreto National High School. He wasadmitted last September 25, 2009 at the Caraga RegionalHospital after being referred by the Loreto District

Hospital. His chief complaint upon admission was suddenonset of weakness on both legs.

Guillain-Barre Syndrome is a serious disorder requiringprompt medical attention which can even be a medicalemergency. However, most Filipinos have not even heardof such a condition. Yes, it is a rare condition, but moreand more Filipinos are struck by it.Hence, our group decided to present this case with theearnest intention to acquire sufficient and accurateinformation about the disorder for us to be able to playour part on the prevention of the said disorder throughinformation dissemination. As future nurses, we

understand the indispensable role of health promotion in


6/22


7/22

u a n- arr syn rome causes progress ve musc eweakness and paralysis (the complete inability to use aparticular muscle or muscle group), which develops overdays or up to four weeks, and lasts several weeks or evenmonths.

Description

The classic scenario in GBS involves a patient who has just recovered from a typical, seemingly uncomplicatedviral infection. Symptoms of muscle weakness appearone to four weeks later. The most common precedinginfections are cytomegalovirus, herpes, Epstein-Barrvirus, and viral hepatitis. A gastrointestinal infection with

the bacteria Campylobacter jejuni is also common andmay cause a severe type of GBS from which it isparticularly difficult to recover. About 5% of GBS patientshave a surgical procedure as a preceding event. Patientswith lymphoma, systemic lupus erythematosus, or AIDS

have a higher than normal risk of GBS. Other GBSpatients have recently received an immunization, whilestill others have no known preceding event. In 197677,there was a vastly increased number of GBS cases amongpeople who had been recently vaccinated against the

Swine flu. The reason for this phenomenon has neverbeen identified, and no other flu vaccine has caused such


8/22


9/22

er p era nerves an sp na roo s are emajor sites of demyelination, but cranial nerves may Themixed type destroys both axons and myelin.

Long-term paralysis in some GBS patients is thought to be

caused by permanent damage to both axons and myelinsheaths. also be involved.

e system's attack on the peripheral nerve cells starts a chain r

truction of nerve insulationThe immune system is responsible for the production ofspecial proteins, the antibodies or immunoglobulins (Ig), as

part of the body's normal defence mechanism. Theseantibodies are produced in reaction to the presence ofantigens, or introduced particles in the body, such asvarious bacteria and vira. Antibodies match specificantigens, and when the two come in contact, they bind

together and a number of destructive reactions occur.

In GBS patients, antibodies are somehow produced againstmyelin. They circulate in the blood seeking myelin, which isfound in nerve cells.


10/22

, ,transmit signals between nerve cells. Some axons aresurrounded by a myelin sheath, a little like electricalcables are surrounded by plastic. The myelin sheathinsulates and protects the nerve cells. It also increases

both the speed and the distance over which nerve signalscan be transmitted. For example, signals from the brain tomuscles are transmitted at a speed of over 50 km/h!

Fig.1: Longitudinal section of an axon and its myelin sheath.The axon is part of nerve cell 1, stretching toward nerve cell2. The myelin sheath resembles tape, wrapped around the

axon in several layers.Myelin does not cover the axon in an uninterrupted tube,like an electrical cable. Instead, it resembles long beadson a string, with space between the beads (see figureabove). The spaces are known as Ranvier Nodes. Axons

are uncovered between these nodes of Ranvier and are


11/22

the nodes, and the more nodes there are, the slower thesignal becomes. This fact is important whenunderstanding recovery - increased numbers of Ranviernodes may be produced during nerve recovery, slowing

signal transmission.

The myelin-attacking antibodies produced in the GBSpatient circulate in the blood and eventually find myelin.They attack and destroy it with the help of white bloodcells, producing inflammation in the nerves. The inflamedcells in turn secrete chemicals that affect the Schwanncells. These cells produce the fatty materials required toproduce myelin. Affecting Schwann cells reduces myelin

production, and some of them may even die, furtherreducing myelin production, while at the same time theexisting myelin is destroyed by the antibodies.As the attack progresses, the peripheral nerve network isgradually destroyed. Motor, sensory or autonomic nervesare attacked, signals are slowed down, blocked or

disrupted and the patient's body is affected accordingly.If the signal transmission speed of a motor nerve isreduced, the patient experiences weakness in the bodyarea controlled by the nerve.

If the signal speed is reduced further, or blocked, thepatient can become paralysed. Similarly, attacks onsensory or autonomic nerves result in disturbances of the


12/22

rom e o y, an ese may e srup e . s resu s nparts of the body feeling numb, as well as strange sensations

of pain, tingling, and pins and needles.

Signals to and from the arms and legs must travel furthest

from the brain and spinal cord, and are therefore mostsusceptible to a barrage of disturbances while en route. Thisis why hands and feet are usually the first body areas that

display GBS symptoms.ck on the peripheral nerves

All the nerves in the human body, with the exception ofthe brain and spinal cord, belong to the peripheral groupof nerves. i.e. the peripheral nervous system comprisesmost of the cranial nerves and the spinal nerves (sensory,motor, autonomic, and mixed).

The peripheral nerves transmit signals from the brain and

spinal cord to, and from, the muscles, organs and skin.Depending on their function, the nerves can be classified asmotor, sensory and autonomous (involuntary) peripheralnerves.

When the immune system malfunctions temporarily and


13/22

When the immune system malfunctions temporarily andGBS sets in, an attack is launched on the peripheralnerves, damaging them. This causes sensorydisturbances, progressive weakening and/or acuteparalysis. Metaphorically speaking, the nervous system

short-circuits. Exactly how the nerves are damaged isdescribed below.

Only the peripheral nervous system is affected, which iswhy GBS is also known as "peripheral neuropathy".

Causes and symptomsThe cause of the weakness and paralysis of GBS is the lossof myelin, which is the material that coats nerve cells (theloss of myelin is called demyelination). Myelin is aninsulating substance which is wrapped around nerves inthe body, serving to speed conduction of nerve impulses.Without myelin, nerve conduction slows or stops. GBS hasa short, severe course. It causes inflammation anddestruction of the myelin sheath, and it disturbs multiplenerves. Therefore, it is considered an acute inflammatorydemyelinating polyneuropathy.


14/22

problem is autoimmune in nature. An autoimmunedisorder is one in which the body's immune system,trained to fight against such foreign invaders as virusesand bacteria, somehow becomes improperly programmed.The immune system becomes confused, and is not able todistinguish between foreign invaders and the body itself.Elements of the immune system are unleashed againstareas of the body, resulting in damage and destruction.For some reason, in the case of GBS, the myelin sheathappears to become a target for the body's own immune

system.

The first symptoms of GBS consist of muscle weakness(legs first, then arms, then face), accompanied by prickly,tingling sensations (paresthesias). Symptoms affect both

sides of the body simultaneously, a characteristic thathelps distinguish GBS from other causes of weakness andparesthesias. Normal reflexes are first diminished, thenlost. The weakness eventually affects all the voluntarymuscles, resulting in paralysis. When those musclesnecessary for breathing become paralyzed, the patientmust be placed on a mechanical ventilator which takesover the function of breathing. This occurs about 30% ofthe time. Very severely ill GBS patients may havecomplications stemming from other nervous systemabnormalities which can result in problems with fluid

balance in the body, severely fluctuating blood pressure,

Diagnosis of GBS is made by looking for a particular


15/22

Diagnosis of GBS is made by looking for a particularcluster of symptoms (progressively worse muscleweakness and then paralysis), and by examining the fluidthat bathes the brain and spinal canal throughcerebrospinal fluid (CSF) analysis.

This fluid is obtained by inserting a needle into thelower back (lumbar region). When examined in alaboratory, the CSF of a GBS patient will reveal a greater-than-normal quantity of protein, with normal numbers ofwhite blood cells and a normal amount of sugar.

Electrodiagnostic studies may show slowing or block ofconduction in nerve endings in parts of the body otherthan the brain. Minor abnormalities will be present in 90%of patients.

Diagnosis

Diagnostic tests

Lumbar Puncture

A needle is inserted in between the bones of the lower back into the fluid around

the spinal cord. A small amount of spinal fluid is taken and the protein level is

tested. In GBS, the protein level is usually increased.


16/22

Electromyogram (EMG or Electromyography)

A thin-needle electrode is inserted into the muscle to betested and electrodes are placed on the skin over

peripheral nerves. This test helps to determine if theperipheral nerves are not communicating between thebrains and muscles in the body.

Nerve Conduction Study (NCS)

Two electrodes are taped to the skin in the affected area

of the patient's body. A small shock is then passedthrough to measure the electrical impulses from oneelectrode to the other. This test records how long it takesfor the electrical impulse to travel from one electrode toanother. If the impulse is slow, it suggests nerve damage

Treatment

There is no direct treatment for GBS. Instead, treatments

are used that support the patient with the disabilitiescaused by the disease. The progress of paralysis must becarefully monitored, in order to provide mechanicalassistance for breathing if it becomes necessary. Carefulattention must also be paid to the amount of fluid the

patient is taking in by drinking and eliminating byurinatin . Blood ressure heart rate and heart rh thm


17/22

course of GBS, has been shown to shorten the course andseverity of GBS. Plasmapheresis consists of withdrawingthe patient's blood, passing it through an instrument thatseparates the different types of blood cells, and returningall the cellular components (red and white blood cells andplatelets) along with either donor plasma or amanufactured replacement solution. This is thought to ridthe blood of the substances that are attacking thepatient's myelin.It has also been shown that the use of high doses ofimmunoglobulin given intravenously (by drip through a

needle in a vein) may be just as helpful as plasma-pheresis.

Immunoglobulin is a substance naturallymanufactured by the body's immune system in response to

various threats.

It is interesting to note that corticosteroidmedications (such as prednisone), often the mainstay ofanti-autoimmune disease treatment, are not onlyunhelpful, but may in fact be harmful to patients with GBS.


18/22

About 85% of GBS patients make reasonably goodrecoveries. However, 30% of adult patients, and a greater

percentage of children, never fully regain their previouslevel of muscle strength. Some of these patients sufferfrom residual weakness, others from permanent paralysis.About 10% of GBS patients begin to improve, then suffer arelapse. These patients suffer chronic GBS symptoms.About 5% of all GBS patients die, most from cardiac

rhythm disturbances.

Prognosis

Because so little is known about what causes GBS to

develop, there are no known methods of prevention.

Prevention


19/22


20/22


21/22


22/22

sinco mark

Documents